Emotional Facial Paresis Research Articles

Emotional Facial Paresis in Temporal Lobe Epilepsy.

Emotional Facial Paresis in Temporal Lobe Epilepsy.

Location of emotional corticobulbar tract in the internal capsule

Emotional facial paresis (EFP) is a rare neurological symptom with intact volitional facial movement. The exact location of emotional corticobulbar tract remains unclear. EFP was frequently recognized following the surgery of stereotactic radiofrequency thermocoagulation for hypothalamic hamartoma in 84.5% of 58 patients. To examine our hypothesis that EFP might be caused by stereotactic trajectories passing through an area including the internal capsule (IC), topographical locations of trajectories were analyzed and compared between the EFP-positive group (n = 41) and the EFP-negative group (n = 8). In the EFP-positive group, multiple (2 to 5) trajectories focused within the genu of the IC in 31 (75.6%) cases, whereas a single trajectory passed through the genu in 8 (19.5%) cases. In the EFP-negative group, 6 (75.0%) of 8 patients had a single trajectory and only one patient had two trajectories passing through the genu of the IC. The ratio between multiple trajectories and a single trajectory relevant to the genu differed significantly between two groups (p < 0.01). The multiple trajectories focusing in the genu have high risks of EFP, whereas a single trajectory seemed to incidentally cause EFP. The results proved our hypothesis and provided a high probability that the emotional corticobulbar tract passes through the genu rather than anterior or posterior limbs of the IC. The location of the emotional corticobulbar tract is in the genu of the IC.

Eating seizures and emotional facial paresis: evidence suggesting the amygdala is a common anatomophysiological substratum

The medial basotemporal lobes (hippocampus, amygdala, parahippocampal gyrus) are considered to be parts of the system responsible for nonvolitional facial movements. In patients with temporal lobe epilepsy, lower facial weakness during emotional expression has been found to occur almost exclusively contralateral to the temporal lobe with the epileptogenic focus. Repetitive and chronic stimulation of the amygdala during eating has also been postulated as a probable mechanism for eating seizures. The authors present the illustrative aspects of both facial asymmetry and eating seizures in a case of mesial temporal lobe epilepsy (MTLE). This report provides evidence that the amygdala may be the common anatomical basis for three different aspects of this patient: emotional facial paresis, eating seizures, and sleep paroxysmal microarousals.

Vascular syndromes of the thalamus.

This article reviews the anatomy, connections, and functions of the thalamic nuclei, their vascular supply, and the clinical syndromes that result from thalamic infarction. Thalamic nuclei are composed of 5 major functional classes: reticular and intralaminar nuclei that subserve arousal and nociception; sensory nuclei in all major domains; effector nuclei concerned with motor function and aspects of language; associative nuclei that participate in high-level cognitive functions; and limbic nuclei concerned with mood and motivation. Vascular lesions destroy these nuclei in different combinations and produce sensorimotor and behavioral syndromes depending on which nuclei are involved. Tuberothalamic territory strokes produce impairments of arousal and orientation, learning and memory, personality, and executive function; superimposition of temporally unrelated information; and emotional facial paresis. Paramedian infarcts cause decreased arousal, particularly if the lesion is bilateral, and impaired learning and memory. Autobiographical memory impairment and executive failure result from lesions in either of these vascular territories. Language deficits result from left paramedian lesions and from left tuberothalamic lesions that include the ventrolateral nucleus. Right thalamic lesions in both these vascular territories produce visual-spatial deficits, including hemispatial neglect. Inferolateral territory strokes produce contralateral hemisensory loss, hemiparesis and hemiataxia, and pain syndromes that are more common after right thalamic lesions. Posterior choroidal lesions result in visual field deficits, variable sensory loss, weakness, dystonia, tremors, and occasionally amnesia and language impairment. These vascular syndromes reflect the reciprocal cerebral cortical-thalamic connections that have been interrupted and provide insights into the functional properties of the thalamus.

Emotional facial paresis in temporal lobe epilepsy: its prevalence and lateralizing value

The selection of patients with medically refractory temporal lobe epilepsy (TLE) for surgery depends on the concordance of data from clinical, imaging and electroencephalographic evaluation. Though clinical examination is often normal, emotional facial paresis has been described in patients with TLE. Utilizing a well-characterized group of mesial TLE (MTLE) patients, who have achieved excellent seizure outcome following anterior temporal lobectomy with amygdalohippocampectomy (ATL), we investigated the prevalence, predictive value and associations of emotional facial paresis. When compared to 8 out of 50 control subjects (16%), 36 out of 50 MTLE patients (72%) exhibited unilateral emotional facial paresis; the difference was highly significant ( P<0.0001). The presence of contralateral emotional facial paresis correctly predicted the side of ATL in 86.1% patients. The occurrence of emotional facial paresis was significantly associated with longer duration of epilepsy prior to ATL and left ATL. Our observations confirm that emotional facial parersis contralateral to the side of mesial temporal sclerosis (MTS) is a valuable localizing sign in correctly predicting the epileptogenic temporal lobe. We hypothesize that the presence of an intact right hemisphere and pathological changes more extensive than MTS may be required for emotional facial paresis to readily manifest.

Emotional facial paresis with striatocapsular infarction

Emotional facial paresis (EFP) refers to hemifacial paresis of emotionally evoked or spontaneous smiling or weeping with preserved volitional movements of the face. The anatomical location for this phenomenon has been controversial. We report a 15-year-old boy with EFP. Follow-up MRI demonstrated infarction limited to the head of the caudate, putamen and anterior limb of the internal capsule on the contralateral side. This case lends support for selective damage at a striatal or capsular site in the production of EFP.